| pubmed-article:3025594 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3025594 | lifeskim:mentions | umls-concept:C0038975 | lld:lifeskim |
| pubmed-article:3025594 | lifeskim:mentions | umls-concept:C0028778 | lld:lifeskim |
| pubmed-article:3025594 | lifeskim:mentions | umls-concept:C1167117 | lld:lifeskim |
| pubmed-article:3025594 | lifeskim:mentions | umls-concept:C0034286 | lld:lifeskim |
| pubmed-article:3025594 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:3025594 | pubmed:dateCreated | 1987-2-10 | lld:pubmed |
| pubmed-article:3025594 | pubmed:abstractText | UV light produces lesions, predominantly pyrimidine dimers, which inhibit DNA replication in mammalian cells. The mechanism of inhibition is controversial: is synthesis of a daughter strand halted at a lesion while the replication fork moves on and reinitiates downstream, or is fork progression itself blocked for some time at the site of a lesion? We directly addressed this question by using electron microscopy to examine the distances of replication forks from the origin in unirradiated and UV-irradiated simian virus 40 chromosomes. If UV lesions block replication fork progression, the forks should be asymmetrically located in a large fraction of the irradiated molecules; if replication forks move rapidly past lesions, the forks should be symmetrically located. A large fraction of the simian virus 40 replication forks in irradiated molecules were asymmetrically located, demonstrating that UV lesions present at the frequency of pyrimidine dimers block replication forks. As a mechanism for this fork blockage, we propose that polymerization of the leading strand makes a significant contribution to the energetics of fork movement, so any lesion in the template for the leading strand which blocks polymerization should also block fork movement. | lld:pubmed |
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| pubmed-article:3025594 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:3025594 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:3025594 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3025594 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:3025594 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:3025594 | pubmed:author | pubmed-author:EdenbergH JHJ | lld:pubmed |
| pubmed-article:3025594 | pubmed:author | pubmed-author:BergerC ACA | lld:pubmed |
| pubmed-article:3025594 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3025594 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:3025594 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3025594 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3025594 | pubmed:pagination | 3443-50 | lld:pubmed |
| pubmed-article:3025594 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:3025594 | pubmed:year | 1986 | lld:pubmed |
| pubmed-article:3025594 | pubmed:articleTitle | Pyrimidine dimers block simian virus 40 replication forks. | lld:pubmed |
| pubmed-article:3025594 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3025594 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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